Clinical Scenarios in Chronic Kidney Disease: Cystic Renal Diseases

Author(s):  
Mario Meola ◽  
Sara Samoni ◽  
Ilaria Petrucci
Toxins ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 367 ◽  
Author(s):  
Wen-Chih Liu ◽  
Yasuhiko Tomino ◽  
Kuo-Cheng Lu

Uremic toxins, such as indoxyl sulfate (IS) and p-cresol, or p-cresyl sulfate (PCS), are markedly accumulated in the organs of chronic kidney disease (CKD) patients. These toxins can induce inflammatory reactions and enhance oxidative stress, prompting glomerular sclerosis and interstitial fibrosis, to aggravate the decline of renal function. Consequently, uremic toxins play an important role in the worsening of renal and cardiovascular functions. Furthermore, they destroy the quantity and quality of bone. Oral sorbent AST-120 reduces serum levels of uremic toxins in CKD patients by adsorbing the precursors of IS and PCS generated by amino acid metabolism in the intestine. Accordingly, AST-120 decreases the serum IS levels and reduces the production of reactive oxygen species by endothelial cells, to impede the subsequent oxidative stress. This slows the progression of cardiovascular and renal diseases and improves bone metabolism in CKD patients. Although large-scale studies showed no obvious benefits from adding AST-120 to the standard therapy for CKD patients, subsequent sporadic studies may support its use. This article summarizes the mechanisms of the uremic toxins, IS, and PCS, and discusses the multiple effects of AST-120 in CKD patients.


2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Amir Taherkhani ◽  
Reyhaneh Farrokhi Yekta ◽  
Maede Mohseni ◽  
Massoud Saidijam ◽  
Afsaneh Arefi Oskouie

AbstractChronic Kidney Disease (CKD) is a global health problem annually affecting millions of people around the world. It is a comprehensive syndrome, and various factors may contribute to its occurrence. In this study, it was attempted to provide an accurate definition of chronic kidney disease; followed by focusing and discussing on molecular pathogenesis, novel diagnosis approaches based on biomarkers, recent effective antigens and new therapeutic procedures related to high-risk chronic kidney disease such as membranous glomerulonephritis, focal segmental glomerulosclerosis, and IgA nephropathy, which may lead to end-stage renal diseases. Additionally, a considerable number of metabolites and proteins that have previously been discovered and recommended as potential biomarkers of various CKDs using ‘-omics-’ technologies, proteomics, and metabolomics were reviewed.


2020 ◽  
Vol 66 (8) ◽  
pp. 1100-1107
Author(s):  
Sibel Gökçay Bek ◽  
Berna Üstüner ◽  
Necmi Eren ◽  
Zeynep Sentürk ◽  
Betül Kalender Gönüllü

SUMMARY BACKGROUND Hepcidin is an important regulator of iron homeostasis. OBJECTIVES This cross-sectional study was conducted to evaluate the association between hepcidin and components of metabolic syndrome in patients with chronic kidney disease (CKD). DESIGN AND SETTING 103 CKD patients and 59 healthy volunteers were included in the study from the University Hospital. METHODS Serum hepcidin levels were measured by enyzme-linked immunosorbent assay (ELISA) test. As for the study parameters, age, sex, body mass index, renal diseases, serum biochemistry, complete blood count, iron and total iron-binding capacity, ferritin, high-sensitive C-reactive protein (hsCRP), C- reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were evaluated. RESULTS The mean age of the patients was 58.63 ± 11.8 years. Hepcidin level was significantly associated with hypertension and higher uric acid levels (P < 0.05). There was a positive correlation between hepcidin and urea, uric acid, creatinine, ferritin, CRP, ESR, phosphorus, triglyceride, low-density lipoprotein (LDL), proteinuria and albuminuria in 24-hour urine collection. A negative correlation was found between hepcidin and estimated glomerular filtration rate (eGFR), hemoglobin, hematocrit, calcium, 25 OH vitamin D, pH, and bicarbonate levels. CONCLUSION Hepcidin, a well-known hormone regulator of iron metabolism, may play an important role in the pathogenesis of metabolic syndrome in patients with CKD, and further studies might delineate in-depth its potential as a promising early marker in these patients.


F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 186
Author(s):  
Daniel Landau ◽  
Ruth Schreiber ◽  
Anya Kleinman ◽  
Alina Vodonos ◽  
Hannah Shalev

Background: The incidence and prevalence of pediatric chronic kidney disease (p-CKD) in developed countries has previously been estimated to be 12 and 75 cases/106 population respectively, much lower than reports in young adults (age 20-40) (40,000/106). Thus, the extent of p-CKD may be underestimated.Methods: Being the only Pediatric Nephrology center in Southern Israel, we reviewed all detected cases of p-CKD (stages 1-5) between 1994-2008. We then prospectively summarized the incidence and prevalence of CKD between 2009-2010. Results: We retrospectively identified 192 children (53.9% of Bedouin origin, 53.4% males, median diagnosis age: 1 year) with CKD. The prevalence in December 2008 was 795 cases/106 for all CKD stages and 331/106 for CKD stage >2. Calculated incidence for the study period (1994-2008) was 46/106/year. The main CKD etiologies were: hypodysplasia: 35%; obstructive uropathy: 13%; genetic renal diseases: 28% and glomerulonephritis: 15%. The proportions of children in each CKD stage were as follows: stage 1: 50%; stages 2-4: 30%; stage 5: 20%. During a subsequent two-year study period we identified 26 new CKD cases (incidence: 54 cases/106/year). Conclusions: p-CKD rates in our area are higher than reported and maybe even higher if asymptomatic populations are screened. Fifty percent of detected cases have CKD stage 1. This may contribute significantly to CKD beyond the pediatric age.


2021 ◽  
Vol 12 ◽  
Author(s):  
Qing Li ◽  
Changying Xing ◽  
Yanggang Yuan

Chronic kidney disease (CKD) is a common progressive disease that is typically characterized by the permanent loss of nephrons and an eventual decline in glomerular filtration rate. CKD increases mortality and has a significant impact on the quality of life and the economy, which is becoming a major public health issue worldwide. Since current conventional-medicine treatment options for CKD are not satisfactory, many patients seek complementary and alternative medicine treatments including Traditional Chinese Medicine. Herbal medicine is often used to relieve symptoms of renal diseases in the clinic. The kidney is abundant in the number of mitochondria, which provide enough energy for renal function and metabolism. In recent years, a vital role for mitochondrial dysfunction has been suggested in CKD. Mitochondria have become a new target for the treatment of diseases. A growing number of studies have demonstrated herbal medicine could restore mitochondrial function and alleviate renal injury both in vivo and in vitro. In this review, we sum up the therapeutic effect of herbal medicine in CKD via targeting mitochondrial function. This implies future strategies in preventing CKD.


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7113
Author(s):  
Marlene Marisol Perales-Quintana ◽  
Alma L. Saucedo ◽  
Juan Ricardo Lucio-Gutiérrez ◽  
Noemí Waksman ◽  
Gabriela Alarcon-Galvan ◽  
...  

Background Renal diseases represent a major public health problem. The demonstration that maladaptive repair of acute kidney injury (AKI) can lead to the development of chronic kidney disease (CKD) and end-stage renal disease has generated interest in studying the pathophysiological pathways involved. Animal models of AKI–CKD transition represent important tools to study this pathology. We hypothesized that the administration of multiple doses of folic acid (FA) would lead to a progressive loss of renal function that could be characterized through biochemical parameters, histological classification and nuclear magnetic resonance (NMR) profiling. Methods Wistar rats were divided into groups: the control group received a daily intraperitoneal (I.P.) injection of double-distilled water, the experimental group received a daily I.P. injection of FA (250 mg kg body weight−1). Disease was classified according to blood urea nitrogen level: mild (40–80 mg dL−1), moderate (100–200 mg dL−1) and severe (>200 mg dL−1). We analyzed through biochemical parameters, histological classification and NMR profiling. Results Biochemical markers, pro-inflammatory cytokines and kidney injury biomarkers differed significantly (P < 0.05) between control and experimental groups. Histology revealed that as damage progressed, the degree of tubular injury increased, and the inflammatory infiltrate was more evident. NMR metabolomics and chemometrics revealed differences in urinary metabolites associated with CKD progression. The main physiological pathways affected were those involved in energy production and amino-acid metabolism, together with organic osmolytes. These data suggest that multiple administrations of FA induce a reproducible model of the induction of CKD. This model could help to evaluate new strategies for nephroprotection that could be applied in the clinic.


Sign in / Sign up

Export Citation Format

Share Document